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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical and biochemical data obtained in 85 patients with diabetic ketoacidosis (DKA) are presented. DKA is an acute exacerbation of diabetes, a characteristic clinico-biochemical syndrome including increasing thirst, polyuria, adynamia, dryness of the skin and mucous membranes, anorexia, nausea, vomiting, occasionally abdominal pain, Kussmaul's breath, acetone odour in the exhaled air, circulatory collapse, prerenal azotemia, stupor, coma. Glycemia level exceeds 19 mmol/l, blood pH over 7.3. The disease is marked by neutrophilic leukocytosis, blood count shift to the left, elevated blood content of creatinine and urea. It was established that the degree of consciousness abnormality does not always correlate with the degree of the clinico-biochemical manifestations of DKA. During DKA, coma occurs relatively seldom (5.9%). It is suggested to use the term "diabetic ketoacidosis", incipient or marked, indicating the degree of consciousness abnormality (stupor, coma).
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PMID:[Diabetic ketoacidosis (causes, clinico-biochemical correlations and terminology problems)]. 644 Dec 97

A phase I trial of chlorozotocin was completed for the single dose every six week schedule. At 250 mg/m2 i.v. push, excessive thrombocytopenia, nausea, and anorexia occurred. Two cases of cholestatic jaundice were seen, and one patient had worsening of his diabetes mellitus after one course. Partial response or prolonged disease stabilization with increased survival was documented in four of seven patients with non-small cell carcinoma of the lung. A starting dose of 225 mg/m2 is recommended for good risk patients with little or no prior bone marrow toxicity from chemotherapy or irradiation. A dose of 200 mg/m2 is recommended for patients with limited previous treatment and good bone marrow reserve.
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PMID:Phase I evaluation of chlorozotocin: single dose every six weeks. 644 79

A 42-year-old woman with a longstanding history of systemic lupus erythematosus and insulin-dependent diabetes mellitus was admitted to the hospital because of icterus, anorexia, pruritus, and weight loss of 3 months duration. During her evaluation the diagnosis of primary sclerosing cholangitis was established. The following case documents the unusual association of systemic lupus erythematosus and insulin-dependent mellitus with primary sclerosing cholangitis.
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PMID:Primary sclerosing cholangitis occurring in a patient with systemic lupus erythematosus and diabetes mellitus. 650 12

The essence of the problem, as previously reported, indicated that few complications of acute appendicitis occur as long as the infection is contained within the appendix, but once the invading bacteria have penetrated the peritoneal appendicular surface or have invaded the regional circulation, any one or more of a series of serious complications can develop. Thus, rightfully, emphasis has been placed upon early removal of the inflamed appendix before penetration has occurred as the best method of preventing complications. We have shown that early appendectomy is predicated on early diagnosis and that diagnostic delay is not limited to extremes of age. The diagnosis may be obscured by an accurate, although misleading, history of prior acute attacks, by precident acute disease, such as viral gastroenteritis and by unimpressive symptoms blunted by intercurrent chronic illness, such as diabetes mellitus. If the elements of periumbilical pain, anorexia, nausea or vomiting and the migration of pain to the right lower abdominal quadrant are contained within the clinical history, one must suspect transmural progression of acute appendicitis; frequent inpatient examinations will allow earliest diagnosis and, thereby, fewest perforations and their attendant serious complications. Misdiagnosis is common. Any patient observed for an ostensibly nonsurgical acute condition of the abdomen who fails to improve markedly during a brief course of appropriate specific or supportive therapy must be thoroughly re-evaluated as a potential surgical candidate. Despite the proliferation of accessible laboratory tests and imaging procedures, the early diagnosis of appendicitis rests upon the clinical skills of the physician. A high index of suspicion is crucial. As Doctor Warfield M. Firor, former senior surgeon commented: "Pain and tenderness at any point where the appendix can lie must raise the diagnostic possibility of appendicitis."
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PMID:Reasons for delay of the diagnosis of acute appendicitis. 670 39

Concurrent diabetes mellitus and hyperadrenocorticism were diagnosed in 30 dogs over a 2-year period. Clinical signs included polyuria, hepatomegaly, polyphagia, abdominal distension, truncal alopecia, anorexia, and vomiting. Because of the similar clinical and laboratory findings for hyperadrenocorticism and diabetes mellitus, hyperadrenocorticism was initially overlooked in some dogs. Insulin resistance, characterized by high daily insulin requirements, developed in the diabetic dogs with untreated hyperadrenocorticism. Therapy with o,p'-DDD resulted in precipitous declines in insulin requirements. By lowering the dosage of o,p'-DDD and supplementing with glucocorticoids during the o,p'-DDD loading period, serious hypoglycemia was avoided. Control of coexisting hyperadrenocorticism lessened the severity of the diabetes mellitus, but insulin therapy remained a necessity in all dogs.
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PMID:Diagnosis and management of concurrent diabetes mellitus and hyperadrenocorticism in thirty dogs. 700 30

Persons with diabetes mellitus often have disordered gastrointestinal function, usually attributed to autonomic neuropathy. Hypoglycemia in persons taking insulin has been considered a possible result of anorexia and gastric atony, but not a potential cause of gastrointestinal symptoms. Three patients with diabetes developing before age 30 yr and of long duration had severe gastrointestinal complaints for 1-9 mo, with symptoms suggesting nocturnal hypoglycemia. All recovered rapidly with no specific treatment other than reduction of insulin doses. Studies identified no gastrointestinal pathology. These patients may represent a subgroup of persons with diabetic enteropathy, in whom recurrent hypoglycemia provokes a reversible derangement of gut function with accompanying symptoms.
Diabetes Care
PMID:Relief of gastrointestinal symptoms by correcting insulin excess. 701 47

The experience with chronic renal failure in two institutions, a tertiary care referral hospital with a high prevalence of diabetes mellitus and a Veterans Administration Hospital, was utilized to formulate guidelines for the nutritional assessment and therapy of chronic renal failure. For optimal nutritional support of patients with renal failure, it is important to characterize objectively nutritional deficiencies. Thus, dietary history, anthropometric measurements (weight/height ratio, arm muscle circumference, and triceps skinfold), and serum protein measurements (total protein, albumin, and transferrin, in particular) provide valuable data concerning the nutritional status of the patient. The serum urea nitrogen to serum creatinine ratio and urea nitrogen appearance are useful for selecting optimal protein intake. The serum urea nitrogen/creatinine ratio must be interpreted with respect to the factors which influence it; i.e., the urea clearance and the urea nitrogen appearance. The goal of nutritional therapy is the preservation of body cell mass and function, fluid, electrolyte, and acid-base homeostasis, mineral balances, and with early use of dialysis, the avoidance of uremic toxicity. Nutritional therapy, especially in patients with superimposed illnesses and associated anorexia, may be enhanced by the use of formula feedings, tube feedings, and, if necessary, total parenteral nutrition.
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PMID:Nutritional assessment and treatment of chronic renal failure. 739 79

Pituitary abscess is relatively rare. Only about 80 cases have been reported. Preexisting lesions in pituitary fossa, such as pituitary adenoma, craniopharyngioma and Rathke's cleft cyst, are inclined to be complicated by infection more than the normal pituitary glands are. We reported a case of pituitary abscess caused by infection of Rathke's cleft cyst. A 67-year-old male had general fatigue and loss of appetite 4 months before admission. On admission he was found to have diabetes mellitus, diabetes insipidus, and hypernatremia. These defects were controlled by medication but he gradually became comatose and febrile. CT and MRI revealed an intrasellar lesion with ring enhancement. Lumbar puncture demonstrated an increase of mononuclear cells and protein. Blood chemistry revealed a marked increase of CRP. He was operated on via the transsphenoidal approach, which revealed sphenoid sinusitis and abscess formation in the pituitary gland. Histological examination of the surgical specimen revealed infection of Rathke's cleft cyst but the fluid in the cyst was sterile. By the drainage of the cyst and the use of antibiotics the patient became alert and signs of infection disappeared. He was discharged with a slight hypopituitarism and returned to normal life. Mortality rate of pituitary abscess is decreasing but is still high because of hypopituitarism and severe infection. Accurate diagnosis and operation are necessary. Transsphenoidal surgery is preferable for postoperative drainage of the abscess.
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PMID:[A case of pituitary abscess caused by infection of Rathke's cleft cyst]. 747 22

The case is recounted of a child who was admitted to hospitals several times over a period of 8 years on account of fictitious illnesses invented by his mother. The first occurred when he was 3.5 years old in January 1984. His mother, a nurse, gave a history of intermittent fever for 3 months, loss of appetite and weight. He had been treated with ampicillin, chloramphenicol, and procaine penicillin. No abnormality was detected and his weight at 15.5 kg was appropriate for his age. No fever was recorded throughout 2 weeks in hospital, but he was given chloroquine for possible malaria and then discharged. At follow-up 6 months later, the mother complained of his wheezing. On examination he was normal and had gained 3.8 kg since discharge. The possibility of vernal conjunctivitis plus asthma was entertained and he was then placed on ketotiphen prophylaxis. There was an uneventful follow-up for 6 months. 5 years later in March 1990, his mother related that he had been treated from 22 January 1988 to 21 November 1989 for tuberculosis with streptomycin, isoniazid, rifampicin, and ethambutol. He was also treated with digoxin and Esidrex-K for suspected rheumatic carditis, after which at the University Teaching Hospital, Enugu, he was investigated from 11 April 1989 to 10 August 1989 and found to be normal. One year later in August 1991 she went to one of the authors complaining about polydypsia, polyphagia, and polyuria. Examination had revealed nothing of note. A clinical assessment for diabetes mellitus found the urine specific gravity persistently at 1.010. He was therefore put on carbamazepine (Tegretol) 100 mg t.i.d. After review by a pediatric nephrologist, the child was declared normal. During this visit, the mother and child were interviewed separately. He believed he was ill because his mother said so. A diagnosis of Munchausen syndrome by proxy was made. The mother was referred back to her doctor to arrange for psychiatric care. In Munchausen syndrome, patients fabricate a variety of symptoms and evidence of illness that have no organic basis. Munchausen syndrome by proxy is a form of child abuse, difficult to diagnose, that could result in death. It is more prevalent in affluent countries with sophisticated medical facilities. Its rarity in developing countries may contribute to the difficulty of detection.
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PMID:Munchausen syndrome by proxy: an experience from Nigeria. 750 55

Due to the progressive clinical course and unchanged poor prognosis of pancreatic cancer supportive therapy has to focus on improvement of the quality of life. Pain control is best achieved with slow release opiates and by chemoablation of the coeliac plexus. Furthermore, management of anorexia with megestrol acetate and tumor-adapted enteral and parenteral nutritional therapy are discussed. The treatment of chemotherapy-induced side effects with haemopoetic growth factors and antiemetics is dealt with as well. Finally, the therapeutic principles of the management of post-pancreatectomy diabetes mellitus and postoperative steatorrhoea are pointed out.
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PMID:[Supportive therapy of pancreatic carcinoma]. 752 56


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